Kyoko Ishii, Yoko Yoshida, Yuji Akechi, Tomohiko Sakabe, Ren Nishio, Remina Ikeda, Kei Terabayashi, Yoshiaki Matsumi, Kazue Gonda, Hideharu Okamoto, Kazuko Takubo, Fumihito Tajima, Hiroyuki Tsuchiya, Yoshiko Hoshikawa, Akihiro Kurimasa, Akihiro Umezawa, Goshi Shiota – 15 April 2008 – Human bone marrow–derived mesenchymal stem cells (BM‐MSCs) are expected to be a potential source of cells for transplantation. Although recent reports have shown that isolated MSCs can differentiate into hepatocytes, the efficiency of differentiation is insufficient for therapeutic application.

Ferdinando Mannello, Klaus Jung – 15 April 2008

Kristiaan Wouters, Patrick J. van Gorp, Veerle Bieghs, Marion J. Gijbels, Hans Duimel, Dieter Lütjohann, Anja Kerksiek, Roger van Kruchten, Nobuyo Maeda, Bart Staels, Marc van Bilsen, Ronit Shiri‐Sverdlov, Marten H. Hofker – 15 April 2008 – Nonalcoholic steatohepatitis (NASH) involves liver lipid accumulation (steatosis) combined with hepatic inflammation. The transition towards hepatic inflammation represents a key step in pathogenesis, because it will set the stage for further liver damage, culminating in hepatic fibrosis, cirrhosis, and liver cancer.

Bo Kyung Kim, Seoung Ok Lim, Yun Gyu Park – 11 April 2008 – The cyclic adenosine monophosphate–response element (CRE)‐transcription factor complex participates in the regulation of viral gene expression and pathologic processes caused by various viruses. The hepatitis B virus (HBV) enhancer I directs liver‐specific transcription of viral genes and contains a CRE sequence (HBV‐CRE); however, whether the HBV‐CRE and CRE‐binding protein (CREB) are required for the HBV life cycle remains to be determined.

Ze‐Zhou Song – 11 April 2008

David van der Poorten, Kerry‐Lee Milner, Jason Hui, Alexander Hodge, Michael I. Trenell, James G. Kench, Roslyn London, Tony Peduto, Donald J. Chisholm, Jacob George – 11 April 2008 – Visceral obesity is intimately associated with metabolic disease and adverse health outcomes. However, a direct association between increasing amounts of visceral fat and end‐organ inflammation and scarring has not been demonstrated.

Ahmed Zaid, Anna Roubtsova, Rachid Essalmani, Jadwiga Marcinkiewicz, Ann Chamberland, Josée Hamelin, Michel Tremblay, Hélène Jacques, Weijun Jin, Jean Davignon, Nabil G. Seidah, Annik Prat – 11 April 2008 – The gene encoding the proprotein convertase subtilisin/kexin type 9 (PCSK9) is linked to familial hypercholesterolemia, as are those of the low‐density lipoprotein receptor (LDLR) and apolipoprotein B. PCSK9 enhances LDLR degradation, resulting in low‐density lipoprotein accumulation in plasma.

Gin‐Ho Lo, Wen‐Chi Chen, Chiun‐Ku Lin, Wei‐Lun Tsai, Hoi‐Hung Chan, Tai‐An Chen, Hsien‐Chung Yu, Ping‐I Hsu, Kwok‐Hung Lai – 11 April 2008 – Both medical therapy and endoscopic variceal ligation (EVL) have proven to be comparable in the prevention of variceal rebleeding. However, the long‐term results are still lacking. Our previous study enrolled 121 patients with history of esophageal variceal bleeding and randomized to receive EVL (EVL group, 60 patients) or drug therapy, nadolol plus isosorbide‐5‐mononitrate (N+I) (N+I group, 61 patients) to prevent variceal rebleeding.

Laurie D. DeLeve, Xiangdong Wang, Yumei Guo – 11 April 2008 – Capillarization precedes hepatic fibrosis. We hypothesize that capillarization of sinusoidal endothelial cells (SEC) is permissive for hepatic stellate cell (HSC) activation and therefore permissive for fibrosis. We examined whether freshly isolated SECs prevent activation of HSCs and promote reversion to quiescence, and whether this effect was lost in capillarization. HSCs were cultured alone or co‐cultured with differentiated or capillarized SECs.

Xiao‐Ming Yin, Wen‐Xing Ding, Wentao Gao – 7 April 2008 – A great part of our current understanding of mammalian macroautophagy is derived from studies of the liver. The term “autophagy” was introduced by Christian de Duve in part based on ultrastructural changes in rat liver following glucagon injection. Subsequent morphological, biochemical, and kinetics studies of autophagy in the liver defined the basic process of autophagosome formation, maturation, and degradation and the regulation of autophagy by hormones, phosphoinositide 3‐kinases, and mammalian target of rapamycin.